Jordi Camps obtained his Ph.D. degree in cell biology from The Autonomous University of Barcelona, Barcelona, Spain in 2005. Right after his Ph.D. completion, he moved to the Laboratory of Dr. Thomas Ried to start his Postdoctoral stage at the National Cancer Institute at the National Institutes of Health in Bethesda, Md, USA. Early in 2011, he became a Research Fellow at the National Cancer Institute. The study of the genomic imbalances in a variety of different diseases, including cancer, is a major step towards the understanding of disease development. In cancer cells, for example, DNA copy number increases have been shown to be one of the mechanisms by which oncogenes and drug resistance genes can be activated, whereas loss of DNA material may cause inactivation of tumor suppressor genes. Knowledge of copy-number aberrations can have also immediate clinical use in diagnosis and, in some cases, can provide useful prognostic information. One of the main research topics in our laboratory is based on the analysis of the genomic imbalances in solid tumors. Our aim is to identify the correlation between the gene dosage and the levels of transcript message. To address this question we use high-density oligonucleotide-based CGH microarrays together with gene expression microarrays. Colorectal cancer holds specific aneuploidies that might represent obligate events for its tumorigenesis. So far, specific genes have been identified as target genes that selectively lead to the gain or loss of chromosomes. Nevertheless, some trisomies are not yet associated to any specific cancer genes. Based on genomic and transcriptional profiling of primary colon and rectum tumors, we inferred what genes might be important for colorectal carcinogenesis upon functional analysis using RNAi on cell lines and mouse models.
Biography Updated on 10 April 2012